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Physiology and Pathophysiology of Skin (2nd Edition)
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Physiology and Pathophysiology of Skin (2nd Edition)

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Physiology".

Deadline for manuscript submissions: 31 May 2027 | Viewed by 1275

Editor

Dr. Seon-Pil Jin

E-Mail Website
Guest Editor
Department of Dermatology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea
Interests: skin; dermatology; scleroderma; rheumatic skin disease; pemphigus; atopic dermatitis; inflammatory skin disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue on the “Physiology and Pathophysiology of Skin” is a comprehensive exploration of the intricate workings and disorders of the body’s largest organ, the skin. This collection of articles brings together cutting-edge research in the fields of dermatology, biology, and physiology, providing invaluable insights into the mechanisms governing skin health and the pathological conditions that disrupt its equilibrium.

This Special Issue delves into the multifaceted aspects of skin physiology, encompassing topics such as epidermal barrier function, wound healing, melanogenesis, immune responses, and sensory perception. Moreover, it illuminates the underlying molecular and cellular processes maintaining skin homeostasis. In parallel, this Special Issue meticulously examines various skin disorders, including dermatitis, psoriasis, atopic dermatitis, and autoimmune diseases, shedding light on the underlying mechanisms, diagnostic tools, and therapeutic approaches.

With contributions from leading experts in the field, this Special Issue is a critical resource for researchers, doctors, and students aiming to deepen their understanding of skin health, from the molecular level to applications. It serves as a foundation for advancing the fields of dermatology and skin biology.

This Special Issue promises to enrich our skin biology and pathology knowledge, ultimately leading to improved diagnostics and therapies for various skin-related conditions.

Dr. Seon-Pil Jin
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • epidermal barrier
  • melanogenesis
  • wound healing
  • skin immunity
  • sensory perception
  • dermatitis
  • psoriasis
  • atopic dermatitis
  • autoimmune skin disorders
  • therapeutic approaches

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Related Special Issue

Published Papers (1 paper)

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Research

12 pages, 2456 KB  
Article
Lysine Carboxymethyl Cysteinate (LCC) Protects the Epidermis from UVB-Induced Barrier Damage Through the Activation of Autophagy
by Xue Xiao, Hong Zhang and Xuelan Gu
Biology 2026, 15(8), 601; https://doi.org/10.3390/biology15080601 - 10 Apr 2026
Viewed by 972
Abstract
Lysine carboxymethyl cysteinate (LCC) has been identified as a glutathione (GSH) precursor for the use of cosmetic products, providing a defense against oxidative stress by elevating GSH levels, and mitigating UVB-induced pigmentation and barrier disruption. In this study, the protective efficacy of LCC [...] Read more.
Lysine carboxymethyl cysteinate (LCC) has been identified as a glutathione (GSH) precursor for the use of cosmetic products, providing a defense against oxidative stress by elevating GSH levels, and mitigating UVB-induced pigmentation and barrier disruption. In this study, the protective efficacy of LCC on epidermal barrier integrity under UVB irradiation was systematically evaluated and its underlying mechanisms were investigated. Results from the UVB-exposed 3D living skin equivalent model (LSE) indicated that LCC effectively restored UVB-induced reductions in epidermal living cell thickness by 9.67%. In addition, LCC markedly increased the expression of key biomarkers related to cornified envelope (CE) formation and skin hydration, including transglutaminase 1, involucrin, loricrin and aquaporin 3 by 104.80%, 121.67%, 218.63% and 388.39%, respectively, compared with the UVB group. Transcriptomics analysis in human primary keratinocytes further revealed that LCC regulated multiple biological functions, including glutathione synthesis pathway, oxidation response, inflammatory process, and notably autophagy. After confirming LCC’s potential in boosting autophagy-associated gene expression (p-value < 0.05) and autophagy activity (p-value < 0.01) in keratinocytes, functional validation in the same model confirmed that LCC counteracted UVB-induced suppression of genes involved in barrier formation, particularly those associated with CE development and autophagy, while these protective effects were abolished by chloroquine, an autophagy inhibitor. Findings from the UVB-exposed LSE model further substantiated this mechanism. Collectively, these results demonstrate that LCC safeguards the epidermis from UVB-induced cornification abnormalities through the activation of autophagy. Full article
(This article belongs to the Special Issue Physiology and Pathophysiology of Skin (2nd Edition))
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